Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 134 patients with chronic active liver disease, selected by identical clinical, biochemical and morphologic criteria, assigned to standard treatment programs and followed at regular intervals, 21 of 105 failed treatment with standard regimens containing steroids. Treatment failure was more common in patients whose serum contained hepatitis B surface antigen, those with more severe liver disease as judged by liver function tests (prothrombin time) and hepatic morphology (subacute hepatitis or cirrhosis). Early diagnosis of treatment failure, based on changes in liver function tests rather than on clinical features of deterioration, coupled with the immediate administration of higher doses of prednisone with or without higher doses of azathioprine, resulted in disappearance of clinical and biochemical features of disease activity in the majority of patients. These results were greatly superior to those earlier reported by us from patients chosen by identical criteria but treated by conventional measures. However, when endogenous encephalopathy developed the outlook was grave, regardless of previous or subsequent therapy. We recommend that patients at risk for failing conventional treatment be identified early, followed carefully with serial liver function tests, and be treated promptly with higher doses of medication when deterioration occurs.
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PMID:Failure of customary treatment in chronic active liver disease: causes and management. 79 99

Twenty patients with acute fulminant hepatic failure and stage II, III, or IV hepatic encephalopathy attributable to viral hepatitis were studied to assess the risk factors, as well as the affects of vigorous medical management. These patients were treated according to a protocol that directed aggressive medical management of fluid balance with electrolyte solutions, plasma, and blood; acid-base balance; coagulation defects with fresh frozen plasma; blood replacement as needed; dietary protein elimination; and orally administered neomycin sulfate. Among the 20 patients there were eight survivors (40%). Seven of the 13 patients who were positive for the hepatitis B surface antigen (HB-Ag) survived (54%), while one of the seven patients whoe were negative for HB-Ag survived (14%). The stage of encephalopathy on admission did not correlate with survival. Patients under the age of 40 years had a 43% survival rate, while those over 40 years had a 33% survival rate. Conservative but vigorous medical management may improve survival in fulminant hepatic failure.
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PMID:Vigorous medical management of acute fulminant hepatitis. 85 88

To evaluate indications for new therapies such as liver transplantation and antiviral therapy, survival of histologically proven hepatitis B surface antigen (HBsAg)-positive cirrhosis of the liver was assessed in a cohort of 98 patients followed up for a mean of 4.3 years. The overall survival probability was 92% at 1 year, 79% at 3 years, and 71% at 5 years. Variables significantly associated with the duration of survival were age, serum aspartate aminotransferase levels, presence of esophageal varices, and all five components of the Child-Pugh index (bilirubin, albumin, coagulation factors, ascites, encephalopathy). Multivariate analysis showed that only age, bilirubin, and ascites were independently related to survival. Survival of patients with decompensated cirrhosis (determined by the presence of ascites, jaundice, encephalopathy, and/or a history of variceal bleeding) and those with compensated cirrhosis at 5 years was 14% and 84%, respectively. For patients with compensated liver cirrhosis, hepatitis B e antigen (HBeAg) positivity was also a prognostic factor with a 5-year survival of 72% for HBeAg-positive cirrhosis and 97% for HBeAg-negative cirrhosis; the risk of death was decreased by a factor of 2.2 when HBeAg seroconversion occurred during follow-up. It is concluded that liver transplantation should be considered for patients with decompensated HBsAg-positive liver cirrhosis and antiviral therapy for patients with HBeAg-positive compensated cirrhosis.
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PMID:Survival and prognostic indicators in hepatitis B surface antigen-positive cirrhosis of the liver. 142 89

Because of the inhomogeneous prognosis in fulminant hepatic failure, prognostic criteria are required which help to establish the indication for liver transplantation as a successful therapeutic procedure. In our study of 33 patients with fulminant hepatic failure (94% viral hepatitis, 67% hepatitis B), serum bilirubin > 320 or < 160 mumol/L, serum creatinine > 110 mumol/L, prothrombin time < 15% of the normal value and duration of jaundice until onset of encephalopathy > 7 days indicated a fatal outcome. When criteria described by O'Grady et al. were used, only limited predictability was achieved. This, as well as the frequently contradictory results of the few prognostic studies published so far, is probably due to the regional differences in the etiology and the different clinical courses of fulminant hepatic failure.
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PMID:Prognostic indicators in fulminant hepatic failure. 144 4

Cerebral edema is a serious complication of the encephalopathy in fulminant hepatic failure. It is a major cause of death. The mechanisms responsible for its formation are unclear, and the aim of this study was to investigate the ultrastructural appearance of brain capillaries by scanning electron microscopy. Samples of cerebral cortex were obtained immediately after death from nine patients with fulminant hepatic failure (seven cases due to acetaminophen overdose, one caused by hepatitis B and one caused by non-A, non-B hepatitis) by needle biopsy at the site of insertion of an extradural pressure transducer to monitor intracranial pressure. The intercellular tight junctions between capillary endothelial cells were intact. The endothelial cells were swollen, with increased numbers of vesicles and vacuoles. The basement membranes were enlarged and vacuolized and the pericytes had increased numbers of vesicles and vacuoles, indicative of passage of fluid by this route. Marked intracellular swelling of the perivascular astroglial foot processes was present. Thus mainly cytotoxic mechanisms, with cellular swelling, and to a lesser extent vasogenic mechanisms, with altered blood-brain barrier permeability, appear to be involved in the cerebral edema of fulminant hepatic failure.
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PMID:Electron microscopic study of brain capillaries in cerebral edema from fulminant hepatic failure. 159 44

Twelve cases of childhood fulminant hepatitis seen over a 4-year period are described. Six had hepatitis A, five hepatitis B and one non-A non-B hepatitis. Encephalopathy, the cardinal feature of fulminant hepatitis, was usually evident within 2 weeks of onset of illness, and the median duration of illness in fatal cases was 19 days. Deep jaundice, prolongation of the prothrombin time and raised serum ammonia were invariable. Eight children died and the four survivors were critically ill before recovering. Acute viral hepatitis is generally a benign illness in childhood. Although infrequently recorded, fulminant hepatitis may, however, ensue and is associated with a high mortality.
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PMID:Fulminant hepatitis in children: report of 12 cases. 171 18

The clinical features, course and histology of liver in 20 patients; mostly middle aged to elderly females, closely resembling chronic Non A Non B hepatitis is presented. They presented quite late in their disease and therefore, complications such as variceal bleeds, ascites and encephalopathy were frequent. Our patients were negative for hepatitis B and C virus serology. Metabolic and immune causes of chronic liver disease were also ruled out. To the best of our knowledge, this is the first study of its kind elaborating the clinical features, course and histology of liver in chronic Non B Non C hepatitis and raises a number of questions as to the nature of the infecting virus and the epidemiology of disease.
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PMID:Yet another cause of chronic viral hepatitis? 176 73

A 54-year-old man with chronic B hepatitis was treated with interferon alfa. Despite resolution of the hepatitis B viral infection, he experienced severe jaundice, ascites, and encephalopathy. Further work-up showed hyperglobulinemia, chiefly immunoglobulin G, and positive smooth muscle and anti-nuclear antibodies. Because of these "autoimmune" features, the patient was treated with prednisone. One month later, a significant clinical and biochemical improvement was observed. A possible autoimmune mechanism induced by interferon alfa is proposed as the cause for the perpetuation of the necroinflammatory activity.
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PMID:Interferon-induced chronic active hepatitis? 186 Jun 46

In 236 patients with fulminant viral hepatitis (FVH), type B (FBH) was most common (47.5%), followed by non-A non-B hepatitis (FNANB, 44.9%) and hepatitis type A (FAH, 7.6%). The survival rate was significantly higher in the FAH group than in the FBH and FNANB groups (61.1, 36.6 and 18.9% respectively), and was significantly higher in the FBH group than in the FNANB group. In spite of screening for hepatitis B virus (HBV), FBH was prevalent (27 of 41) in post-transfusion cases; this phenomenon is discussed in relation to a recently revealed mutation of HBV. Within a month after the onset of hepatitis symptoms all cases in the FAH, 93% in the FBH and 79% in the FNANB group, developed encephalopathy. When the duration of illness before the onset of encephalopathy was more than 10 days (a subacute form), the survival rate was significantly lower than when encephalopathy developed in less than 11 days (an acute form). This difference could be accounted for by the difference in the relative frequency of aetiological viruses in the two forms and the higher survival rate in the acute, than the subacute, form in the FNANB group.
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PMID:Aetiology and prognosis of fulminant viral hepatitis in Japan: a multicentre study. The Study Group of Fulminant Hepatitis. 191 24

The aetiology of chronic liver disease covers a wide range of congenital or acquired abnormalities of the hepatocellular biochemical network. Although our knowledge has considerably increased in recent years, the aetiology of chronic liver disease often remains obscure. Acquired irreversible disturbances of normal liver function can be mediated by hepatotrophic viruses, chemicals, chronic oxygen depletion, or interference with the immune system. Considerable progress has been made in the detection and characterisation of hepatitis B, C, and D viruses as causative agents of chronic active hepatitis. Alcohol abuse remains the predominant cause of chronic liver disease in the Western world. The targets of autoantibodies used to diagnose autoimmune diseases of the liver and primary biliary cirrhosis continue to be biochemically defined. Their significance for the aetiology of the disease, however, remains to be established. Nonparenchymal cells play an important role in the sequence of events following hepatocellular injury and ultimately leading to liver cirrhosis. They release vasoactive compounds, cytokines, and other important mediators, and participate in the modulation of the extracellular matrix that is characteristic of liver fibrosis and cirrhosis. The biochemical basis of liver cell necrosis remains poorly defined. In spite of recent progress, and the detection of some new pathogenic principles that help in the understanding of the complications of chronic liver disease such as portal hypertension, oesophagogastric variceal bleeding, portosystemic encephalopathy, ascites, and other metabolic disturbances, many questions concerning the aetiology and pathophysiology of chronic liver disease and its complications remain to be answered.
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PMID:Aetiology and pathophysiology of chronic liver disorders. 208 79


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